The introduction of high-resolution structural brain imaging and new analysis methods has led to signif- icant improvements in our understanding of the cor- relations between the anatomy of cerebellar lesions and the observed clinical deficits (Rorden & Karnath, 2004). Signal-to-noise ratio on MRI increases with increasingfield strength and now allows spatial res- olution in the submillimeter range (Timmann et al., 2009).
1
1 2
3 4
5 6
7 Dentate
Interposed Posterolateral
fissure
Nodulus Flocculus
Paraflocculus lobule Biventer lobule
Gracile lobule Superior semilunar lobule Posterior quadrang, lobule Anterior quadrang, lobule
Central lobe Fissures and lobules
Lingula
I IV V VI VII VIII Uvula
IX
VI VII Tonsil
Tonsil X II, III
Primary fissure
Inferior semilunar lobule Fastigial
A
B
Figure 3.7 Lesion symptom mapping. (A) Cerebellar lobules shown on an unfolded cerebellum. (B) Lesion-symptom mapping.
Schematic sketch of findings in patients with focal cerebellar lesions. The figure summarizes the results of lesion-symptom mapping in studies on eyeblink conditioning, cerebellar ataxia rating scores, balance in stance and gait, and upper and lower limb coordination. 1: ataxia of stance/gait; 2: lower limb ataxia; 3: upper limb ataxia; 4: dysarthria; 5: limb ataxia; 6: conditioned eyeblink response (CR) timing; 7: CR acquisition. Adapted from: Timmann et al.,2008. (Seecolor section).
Lesion-based MRI subtraction analysis shows that the fastigial nuclei (and to a lesser degree the interposed nuclei) are more frequently affected in patients with impaired compared with unimpaired dynamic balance control (Timmann et al., 2009;
Figure 3.7). Also, the interposed and the adjacent dentate nuclei are more frequently affected in patients with impaired leg placement compared with those with non-impaired leg placement. Patients with impaired leg placement abnormalities exhibit diffi- culties in the adaptation of locomotion to additional loads. Recent data show that the intermediate zone appears to be of particular importance for multi-joint limb control both in goal-directed leg movements and in locomotion. Lesions of the intermediate zone may lead to impaired leg and trunk coordination.
48
In cerebellar stroke, a somatotopy of the superior cerebellar cortex is found, in agreement with animal data and functional MRI observations in healthy con- trol subjects (Grodd et al.,2001). Upper limb ataxia is correlated with lesions of cerebellar lobules IV–V and VI. Lower limb ataxia is correlated with lesions of lob- ules III and IV. Dysarthria is correlated with lesions of lobules V and VI. Limb ataxia is correlated with lesions of the interposed and part of the dentate nuclei, and ataxia of posture and gait is correlated with lesions of the fastigial nuclei, including part of interposed nuclei.
Recovery after lesions to the nuclei of the cerebellum is often less complete (Eckmiller & Westheimer,1983).
In cerebellar cortical degeneration, there is a sig- nificant correlation between the cerebellar degen- eration and both International Cooperative Ataxia Rating Scale and Scale for Assessment and Rating of Ataxia scores (see Chapter4). Oculomotor disorders are highly correlated with atrophy of the medial cere- bellum. Posture and gait ataxia subscores show the highest correlations with the medial and intermedi- ate cerebellar volume, whereas impairment in limb kinetic functions correlates with atrophy of lateral and intermediate parts of the cerebellum. Atrophy of the intermediate zone is correlated not only with limb ataxia and dysarthria, but also with ataxia of stance and gait.
For classical conditioning of the eyeblink response, a form of motor learning (see Chapter2), learning rate in healthy subjects is related to the volume of the cor- tex of the posterior cerebellar lobe (Timmann et al., 2008). In patients with focal cerebellar lesions, acquisi- tion of eyeblink conditioning is significantly decreased in lesions that include the cortex of the superior poste- rior lobe, but not the inferior posterior lobe. Impaired timing of conditioned eyeblink responses correlates with lesions of the anterior lobe. A meta-analysis of neuroimaging studies supports the following func- tional topography (Stoodley & Schmahmann,2009):
! Sensorimotor tasks activate the anterior lobe (lobule V) and adjacent lobule VI, with additional foci in lobule VIII. Motor activation is linked with activation in lobules VIIIA/B, and somatosensory activation is confined to VIIIB.
! The posterior lobe is involved in higher-level tasks. Lobule VI and crus I are activated in language and verbal working memory; lobule VI is activated in spatial tasks; lobules VI, crus I, and lobule VIIB are activated in executive functions;
and lobule VI, crus I, and medial VII are activated during emotional processing. Language is
right-lateralized, whereas spatial processing shows a greater lefthemisphere activation. Language and executive tasks activate regions of crus I and lobule VII implicated in prefrontal-cerebellar loops. Emotional processing is associated with activation of the vermal lobule VII, participating in cerebellar-limbic circuitry. Functional neuroimaging investigations support the hypothesis that there is an anterior sensorimotor versus posterior cognitive/emotional dichotomy in the human cerebellum (Stoodley &
Schmahmann,2009). Motor tasks are localized to the anterior lobe, with a secondary representation in lobules VIIIA/B; somatosensory tasks also involve the anterior lobe, with a secondary representation in lobule VIIIB. None of the
“higher-level” language, working memory, spatial, or executive tasks are associated with activation in the anterior lobe.These observations are in agreement with the hypothesis of a double representation of the body in the cerebellum (Snider & Eldred,1951).
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glutamatergic neurons (red arrows). PTF1A-expressing
neuroepithelium (ventricular zone) generates GABAergic neurons (blue arrows). Cells leaving the rhombic lip migrate over the anlage and form an external layer of cells which continue to proliferate. Granule neuron progenitors form the external granular layer (EGL). Inward radial migration of EGL generates the internal granular layer (IGL). Cerebellar Purkinje neurons are post-mitotic as they leave the ventricular zone. Adapted from: Hoshino, 2006.
Paleocerebellum Neocerebellum Achicerebellum
Central lobe
Anterior quadrang. lobe Posterior quadrang. lobe
Superior semi-lunar lobule
Inferior semi-lunar lobule Gracile lobule Biventer lobule Paraflocculus Flocculus Nodulus Posterolateral
fissure
Lingula
Primary fissure
Declive VI
POSTERIOR LOBE Folium VII
Tuber VII
Pyramis VIII Uvula IX PONS
Nodulus X Lingula I Central II-III
Culmen IV-V ANTERIOR LOBE
MEDULLA
OBLONGATA FLOCCULONODULAR LOBE II, IIII
IV, V VI Primary fissure
VII VIII
IX
X Hemisphere Vermis
Primary fissure Posterior superior
Posterolateral fissure Horizontal fissure
Horizontal fissure
Horizontal fissure Flocculus Tonsilla
Nodulus
Nodulus Flocculus Inferior peduncle
Middle Superior peduncle
A B C
D E F
Fourth ventr cle MIDBRAIN
Figure 1.6 Illustration of the human cerebellum. (A) Superior view. The anterior lobe is demarcated from the posterior lobe by the primary fissure. (B) Anterior-inferior view showing the cerebellar peduncles. The flocculonodular lobe, delineated by the posterolateral fissure, is visible. (C) Inferior view showing the posterior part of the posterior lobe and the flocculonodular lobe. (D) Phylogenetic division of the cerebellum in paleocerebellum (medially), neocerebellum (laterally), and archicerebellum (flocculonodular lobe) represented on an unfolded cerebellum. (E) Division in 10 lobules. (F) Components of the vermis. From: Colin et al.,2002. With permission.
Figure 1.7 Parcellation of the cerebellum in individual lobules.
Upper panels, coronal sections; lower left, parasagittal section; lower right, inferior view of the cerebellum.
Figure 1.9 Volume of lobules in percentage of the total estimated cerebellar gray matter volume in healthy adults (total=100%). Volumes of left and right side are considered together. Adapted from: Diedrichsen et al.,2009.
B
pf Bc
Lc
Gc
br. c
CF MF
ST
IO
CN PN
mf
: + : − Gran. c
Sc
Figure 1.10 Wiring and connections of the cerebellar circuitry. (A) Mossy fibers (blue) and climbing fibers (red) project to cerebellar cortex (grey area) and cerebellar nuclei. The Purkinje neuron interacts with granule cells and inhibitory interneurons of the cerebellar cortex. Purkinje cells represent the output of the cerebellar cortex. Purkinje neurons inhibit cerebellar nuclei, which are the origin of the output emerging from the cerebellum. (B) Neurons of cerebellar circuitry. Abbreviations: MF: mossy fiber; CF: climbing fiber; IO: inferior olive; Gran. c: granule cell; br. C: brush cell; Gc: Golgi cell; Lc: Lugaro cell; Bc: basket cell; Sc: stellate cell; pf: parallel fiber; PN: Purkinje neuron; CN: cerebellar nuclei.
+: excitatory; – : inhibitory.
Figure 1.11 The glomerulus. The enlarged extremity of a mossy fiber (represented in yellow), called “rosette,” is connected with dendrites of the granule cells (shown in blue) and a Golgi cell (illustrated in green). It also receives an axonal projection from the latter. Therefore, Golgi cells regulate mossy fiber inputs. Golgi cells are themselves excited by parallel fibers emerging from the granule cells.
Figure 1.12 Imaging of cerebellar nuclei in adults using high-resolution MRI. (A) (a–c) Axial, coronal, and sagittal slices of the human cerebellum and corresponding slices through the high resolution (0.7×0.7×0.7 mm 3 voxels)"(d–f) and T1 (g–i) maps calculated from multi-averaged data requiring 40 min of scan time. The dentate, as well as globose and emboliform nuclei of the interposed nucleus, can be clearly delineated on both the T1 and"maps, allowing their anatomy to be fully appreciated. Arrows indicate the dentate nucleus on each image. (B) Anatomy of the deep cerebellar nuclei. Upper row, the dentate nucleus is composed of two parts: a dorsomedial and rostral region with narrow dentations (microgyric dentate) and a ventrolateral and caudal portion with wide and subdivided gyrations (macrogyric dentate).
Lower picture: identification of the fastigial, globose and emboliform nuclei. (C) Volume renderings of the dentate nuclei of each of 10 adults, superimposed on their corresponding T1 maps. The images are taken from the superior-anterior viewpoint. From: Deoni and Catani,2007.
With permission.
interstitial and Darkschewitsch nuclei). FN also projects to bulbar reticular formation: medial bulbar reticular formation (RFm) and lateral reticular nuclei (LRN), at the origin of the reticulospinal tract (RST). Reticular nuclei project back to cerebellar nuclei
(cerebello-reticulocerebellar loops, not illustrated) and receives afferents from the spinal cord. FN is also connected with the parasolitarius nuclei (PSN) and the perihypoglossal nuclei (PHN). VN projects to the spinal cord via the vestibulospinal tract (VST) and projects back to the FN and the flocculonodular lobe. Interrupted line: midline.
Figure 1.14 Output channels of the dentate nucleus. Distinct areas of the dentate nucleus project predominantly upon different regions of the contralateral cerebral cortex, via thalamic nuclei (MD/VLc: medial dorsal/ventralis lateral pars caudalis nuclei; area X, VPLo: nucleus ventralis posterior lateralis pars oralis). Dorsal portions of the dentate nucleus project mainly upon area 4. With permission from: Manto,2009.
Figure 3.7 Lesion symptom mapping. (A) Cerebellar lobules shown on an unfolded cerebellum. (B) Lesion-symptom mapping.
Schematic sketch of findings in patients with focal cerebellar lesions. The figure summarizes the results of lesion-symptom mapping in studies on eyeblink conditioning, cerebellar ataxia rating scores, balance in stance and gait, and upper and lower limb coordination. 1: ataxia of stance/gait; 2: lower limb ataxia; 3: upper limb ataxia; 4: dysarthria; 5: limb ataxia; 6: conditioned eyeblink response (CR) timing; 7: CR acquisition. Adapted from: Timmann et al.,2008.